COXA PLANA

ARTICLES

COXA

PLANA

By Charles T. Ryder, M.D., John D. LeBouvier, M.D., and Rosamond Kane, M.D.

Department of Orthopaedic Surgery, Columbia University, and the New York Orthopaedic Hospital at the Columbia-Presbyterian Medical Center

(Submitted October 9, accepted October 30, 1956.)

ADDRESS: (C.T.R.), 180 Fort Washington Avenue, New York, New York.

979

Ped #{237}a!

rics

VOLUME 19 JUNE 1957 NUMBER

6

I

N ITS 46 years as a recognized disease,

coxa plana (LegglCalve2Perthes3 dis-ease, pseudocoxalgia, osteochondrosis of the

femoral head, etc.) has evoked a tremendous amount of study and speculation, and a bibliography of some 2,000 items.4 It is

discouraging that all this effort has failed to prove a cause or to find a cure for the disease, and it is perhaps more significant

that it has not yet even produced a name that everyone can agree to use! The most popular term now seems to be coxa plana (“idiopathic” being implied); this is our

preference because it is descriptive,

non-committal and avoids the disputed eponym.

Though never a threat to life, coxa plana

is a menace to limb; this is its significance.

It is exclusively a disease of childhood, but

its serious consequences rarely appear

be-fore adult life. Because coxa plana is a

“new” disease, the nature of these conse-quences is only now coming to

light-in-deed Legg’s first patients are at present in

their fifties.

In the cases currently being studied at the Columbia-Presbyterian and New York Orthopaedic Hospitals, our emphasis has

been on the natural history of the disease.

This paper is based in part on our findings

in 104 patients.

WHAT IS COXA PLANA?

Coxa plana is a disease of the previously normal hip joint in which the bony nucleus

of the femoral head becomes necrotic. The dead bone is gradually replaced by the usual stages of bone repair. During this

pro-cess there is usually some flattening of the normally spherical femoral head. A

sec-ondary deformity of the acetabulum

de-velops with growth. The final result may be

a mechanically imperfect joint subject to the ills of all deformed joints-premature degenerative changes and consequent pain and limitation of motion.

WHO GETS COXA PLANA?

Cases in this series (Table I) show that

a child may develop this disease from the time he becomes a full-fledged biped until

he seriously considers shaving. The

young-est patient was 22 years old when

symp-toms began, the oldest was 136/12 years. Children from 4 to

6 years

of age are particularly vulnerable; just half of all cases

TABLE I

AGE AT ONSET

(Patients with Unilateral Involvement)

None

Limp Pain

Limp and pain (Trauma

1 I

40

25)

980 RYDER -

COXA

PLANA

Age

(yr)

Boys

GirLs Total

? 1 0 1

0-2 0 0 0

2-3 5 0 5

3-4 8 1 9

4-5 11 5 16

5-6 14 2 16

6-7 11 2 13

7-8 4 3 7

8-9 6 2 8

9-10 1 0 1

10-11 2 2 4

11-12 3 1 4

12-13 3 0 3

13-14 1 0 1

who recently studied coxa plana at the Hospital for Joint Diseases, found practi-cally the same age incidence of the disease. There is a notable paucity of coxa plana

in the Negro (Table II). In the series being

reported there is one Negro patient. Goff was able to document only one case despite a search through records of a large Southern hospital. Broder found 7 Negroes in a series of 102 cases of coxa plana studied in a hos-pital with a predominantly Negro

popula-tion. The pedigree of these patients was not given nor could it be obtained in the case of the series reported here. In the

Orient coxa plana is rather common. No cases from the yellow race occur in the present series, but Broder reported one.

Thus with little in common other than

the joint involved, the geographical and

TABLE II

SEX, SIDE INVOLVED AND RACE

Sex Right Left Bilateral Total

Male 32 38 16 86

Female 12 6 0 18

Total 44 44 16 104

Race:Whit e, 103; Neg ro, 1.

racial incidence of coxa plana and congeni-tal dislocation of the hip is strikingly

simi-lar.

Male patients with coxa plana prepon-derate in the ratio of five to one in this series as in that reported by Goff and by

Broder; this is in contrast to the reversed sex incidence of congenital dislocation of

the hip. The scarcity of bilateral disease in girls is striking-no cases out of 16 in

the present series. About one-fifth of the

children had bilateral disease in this series

and in those reported by Goff while only about one-tenth of cases reported by Broder were bilateral.

Right and left hip are affected equally frequently in coxa plana, a second point of dissimilarity with congenital dislocation of the hip. In that condition, involvement of the left hip predominates.

Dr.

Goff

studied

several

general

char-acteristics of the children in his group. He found that they were shorter than average in stature and that their bone ages were low, both observations suggesting an over-all

growth retardation. He also “body-typed” the children by Sheldon’s method and

found a preponderance of mesomorphism in both boys and girls with coxa plana as

compared with the incidence of this trait in normal children. We have no

informa-tion of this sort in this series.

HOW IS COXA PLANA DIAGNOSED?

The first symptoms of this disease are limp or pain in the affected limb, which sometimes occur concomitantly (Table III). A painless limp was notably more

common in the youngest children. Pain

when present was usually mild. It was most

TABLE III

FIRST Smar’roM

ARTICLES 981

frequently felt in the groin or upper thigh,

but several children described it as being in the knee only. This emphasizes a maxim of musculo-skeletal diagnosis: Unexplained pain in the knee may come from the hip. When pain alone was the first symptom, limp almost always developed soon after.

Another maxim is: In musculo-skeletal disease of any kind in children there is often a history of injury. This was true in

one-fourth of our cases-a ratio in good

agreement with Broder but much lower than noted in the experience of others.4’6

So undramatic is the onset of coxa plana that there is a real “lag period” between the first observed symptom and the time when parents decide medical advice should

be sought. This varied widely, from 1 day to nearly 1 year in our cases, with a 3- to

6-month “lag” history being the most

com-mon.

When the child is finally brought to the

doctor, the disease can be diagnosed in almost every instance (Table IV). The physical findings are those of hip joint

irri-tation: a protective limp, pain on forced motion, muscular guarding against motion

(“spasm”), and restriction of motion. Ab-duction and internal and external rotation are characteristically limited. These findings demand roentgenographic examination. In

this series the results were diagnostic in a large majority and completely negative in no case of coxa plana. (Our clinic has

always closely followed patients with un-diagnosed limp or leg pain, as well as

cases of “synovitis of the hip,” for fear of

TABLE IV

CLINICAL FINDINGS-FIRST EXAMINATION

(Patients with Unilateral Involvement)

Limp -almost always, mnil(l to moderate

Pain on hip motion-frequent

“Spasm” -frequent, usually mild

Restricted motion -usual, especially of abduction, and internal and external rotation Atrophy of muscles-uncommon

Shortening -rare

Tenderness -rare

missing early coxa plana or other hip dis-ease. On the whole the parents concerned have co-operated well with this policy.)

Several special points concerned with the initial diagnosis of coxa plana emerged from

the study of 14 patients who had bilateral involvement by roentgenographic

examina-tion when they first appeared at the clinic. Symptoms were strictly unilateral in 12 of these children, and findings were absent

or minimal on the asymptomatic side. Two

cases developed the disease in the second

hip while under treatment for the first; both were asymptomatic and the diagnosis was made by routine roentgenograms taken

to follow the course of the first hip. Coxa plana can in fact be a very “quiet hip

tlis-ease.”

With what seems to be an increasing awareness by parents that the minor limps

and aches of their children may not be merely “growing pains,” we will probably

see a shortening “lag period” in coxa plana, and with it, cases too early to be diagnosed with certainty. The points worth emphasis are: 1) most cases of coxa plana can be

diagnosed easily when they first visit the doctor by clinical and roentgenographic examination; 2) roentgenograms should be

made of both hips at first examination and during treatment, and 3) any child with an

unexplained limp or leg pain should be followed closely.

WHAT IS THE COURSE OF

COXA

PLANA?

Although several authors have described the histopathology of coxa plana as adduced from surgical specimens,7’8 the major work is that of Jonsater.9 He performed a series of femoral-head biopsies, using a punch-,

like instrument, in the several stages of the

disease, as well as a series of hip-joint arthrograms to define and measure the

actual shape of the cartilaginous articula-ting surface of the head. His excellent

report is “must reading” for any student of this disease.

TABLE V

ROENTGENOGUAPII IC STAGES OF (‘oxA PLANA

,1,

3. .,:‘ __________________________

FIG. 1. Initial stage. (1) Roentgenogram shows condensation of

femoral head. (2) Section shows necrotic marrow with bone frag-ments. (3) Section shows bone is totally necrotic with no osteocytes.

(From Jonsater.)

982 RYDER-COXA PLANA

1. Initial } to 1 year

2. Fragmentation t to 3 years

3. Repair 1 to ‘tyears

4. l)efinite

34 to 6

femoral head. Jonsater has simplified

Wal-denstr#{246}m’sbo classification (Table V). In the initial stage, which lasts 6 months to 1 year, the epiphysis is dense, somewhat flattened, and irregular at the margins. There are often cyst-like areas in the neck adjacent

to the epiphysis. Next is the fragmentation

stage, in which the epiphysis is markedly

flattened and divided into many pieces.

This stage lasts 2 to 3 years. Third is the

repair stage, lasting 1 to 2 years, in which

the epiphysis becomes homogeneous.

Finally there is the definite stage. Repair

has been completed and the head shape has

become permanent.

The earliest lesion of coxa plana is un-known, for when tile child first appears, a

drastic event has already occurred in the femoral head. This is an extensive necrosis

of the epiphyseal bone (Fig. 1). Howorthhl has shown in 50 cases treated by operation

that there is also in this plmse a marked inflammation of all the soft tissues of the

hip. Undoubtedly it is this svnovitis that

causes tile early signs and symptoms, for

pain, limp, muscle spasm, and restricted motion are common to inflammation of the

hip joint from whatever cause.

Despite drastic change in the bone, tile

femoral head retains its spherical shape in this phase (Fig. 2).

If a child in this stage is put to bed, the

usual treatment of cases in this series, his

spontaneous pain, if any, disappears within

\

I

j “‘., t

4:-. o’t

ARTICLES 983

FIG. 2. Initial stage. (1 and 2) Roentgenogram shows condensation of head and epiphyseal line is slightly wide and irregular. (3 and 4) Articular surface

is virtually spherical by arthrograni. (From Jonsater.)

a few (lays. Spasm and pain on forcing

motion subside gradually over a variable time, ranging from 2 or 3 weeks to 6 months. Thereafter the disease runs a benign course

clinically, as long as weight-bearing is

avoided.

Tile fragmentation stage, as Jonsater notes, is really a repair phase (Fig. 3).

Ne-crotic bone is still present, but young con-nective tissue with a rich blood supply

dominates the picture, and new bone is being formed. Even in this stage (Fig. 4)

the actual shape of the femoral head is

smooth and only slightly flattened.

It is in the repair phase that tile

de-formity of the femoral head becomes

con-spicuous. This stage is characterized

histo-logically (Fig. 5) by the appearance of normal bone and marrow, though some

necrotic spicules persist. The new connec-tive tissue is less prominent than it is in the

fragmentation stage. The arthrogram shows (Fig. 6) that the articular surface now is dis-tinctly flattened, approximating in shape the regenerating bony epiphyseal nucleus.

Once the repair stage is well established there is no further increase in head

de-formity.

In the definite stage the repair process has restored normal cancellous bone to tile

head, and the articular contour conforms to tile bony contour (Fig. 7). This is the

end of the disease, and the final shape of the hip joint is established. The surfaces

then retain their flattened shape despite any

further growth.

These stages describe the course of coxa

plana, but there is great natural variation

among cases, both in the course of the actual process and in the severity of the residual deformity (Figs. 8 and 9). In some the involvement is mild, and the fragmenta-tion stage can be absent or inconspicuous. The disease runs a short course-around 1

year-and little or no deformity ensues. In other cases the disease localizes in a

seg-ment of the femoral head. Often a good recovery may be expected. In all cases the

re-tH

FIG. 3. Fragmentation stage. (1) Epiphysis is markedly shrunken

and fragmented. (2) Section shows necrotic bone being invaded by

connective tissue. (3) Section shows newly-formed bone. (From

Jonsater.)

984 RYDER - COXA PLANA

viewing a series of films. They are,

how-ever, useful if somewhat inaccurate sign

posts along the way.

Jonsater’s observations bear significantly on therapy. Most important is the fact that

by the time tile patient presents himself, his femoral head is already necrotic-the damage has been done, and all the rest of

the “disease” is actually not a disease at all,

but a process of repair, slow and tedious as is always the nature of bony repair.

“Treatment” therefore can consist only of measures which will facilitate or accelerate bony repair. So far no proven clinical

tech-nique exists.

The second striking factor is joint de-formity, which develops slowly and gradu-ally during repair. It is the only residuum of the disease and tile only cause of trouble

in later years. While the bony femoral head is reforming, any load on the joint, even that produced by mere muscular pull,

can act only to increase the flattening.

WHAT CAUSES COXA PLANA?

Numerous theories about the cause of

FIG. 4. Fragmentation stage. (1 through 4) Spherical articular surface is still quite well maintained despite irregularity of bone. (From Jonsater.)

ARTICLES 985

its histopathology and natural history.

Among these was the theory of Jansen that

a congenital flattening of the joint socket created an incongruent articulation which led to vascular damage. The demonstrated appearance of coxa plana in a hip previ-ously normal in every way refutes this

con-cept.6

Kidner1’ suggested infection as a cause of coxa plana after growing a staphylococ-cus aureus from an operative case and was supported by Phemister” who similarly

grew a hemolytic streptococcus. Several

sur-geons subsequently obtained no growth.

The inability to grow out organisms

con-sistently and the absence of other signs of infection fail to support this theory and it has been abandoned generally.

Durham and Outland’4 suggested that coxa plana, rickets, and osteomalacia “may be related etiologically,” but Buchman15

could find no evidence of disorder in cal-cium and phosphorus metabolism in 50

cases of coxa plana.

A flurry of excitement ensued when

Cava-naugh and associates,’6 later supported by

Schaefer,’ reported finding evidence of

hypothyroidism in cases of coxa plana. A number of children were given thyroid

(none in the series reported here) until Gill’8 demolished the concept by a careful study of thyroid function in 20 patients. The final blow to this theory came from

Katz,’9 who found normal values for pro-tein-bound iodine in 32 children with coxa

plana.

A number of authors, recognizing necro-sis of bone as the essential lesion in coxa plana, have believed that it is specifically

caused by failure of the blood supply to the femoral head. Legg himself held this view, ascribing the vascular changes to trauma.

The peculiarly vulnerable nature of the circulation of the femoral head is well

known. It consists, according to Kolodny

who made extensive anatomic studies,20 of

three groups of vessels. The diaphyseal vessels, few and unimportant, penetrate

FIG. 5. Repair stage. (1) Epiphysis is coalescing; contour is

rounding. (2 and 3) Bone trabeculae are nearly normal. (From

Jonsater.)

FIG. 7. Definite stage. (1 through 4) Bone texture is normal. Entire epiphysis is moderately flattened. (From Jonsater.)

ARTICLES 987

enter tile epiphysis, furnishing the major

blood supply to the head. The vessels of the round ligament have a limited

distribu-tion near the attachment of that structure. The ischemic necrosis concept is of course

subject to some testing in the laboratory.

In a well-conducted experiment, Zemansky

and Lippmann’1 produced anemia, necrosis,

and deformity of the femoral head by divid-ing the epiphyseal vessels and those of the

round ligament in young rabbits. Several

other workers similarly produced ischemic

lesions of greater or lesser degree in animals

by surgical or chemical insult to the vessels of the femoral head.

Current thought seems generally, and we believe reasonably, to accept the theory of

ischemic necrosis. The unanswered question

is: what damages the vessels of the femoral

head? Legg’s opinion that it is trauma,

either isolated or repeated, was supported in part by Sundt. Howorth believed that a mild infectious arthritis is the primary lesion and that it causes sclerosis of the

yes-sels, a view apparently shared by Platt.” Axhausen’s suggestion of bacillary embolism

has received little support.

A provocative hypothesis has recently come from Ponseti.’3 He believes, on the

basis of punch biopsy, that the primary lesion is a faulty epiphyseal plate, and reports that the histopathology of this cartilage in coxa plana closely resembles that produced by feeding aminonitriles to rats. The features of these lesions are fibril-lation and tearing of the cartilage with

ir-regular proliferation of chondrocytes. Pon-seti believes that the epiphyseal vessels are injured as they cross closely over the dis-rupted, weakened epiphyseal plate. The

original damage to the epiphyseal cartilage,

in this view, results from some metabolic aberration (perhaps even aminonitrile

Fic. 8 (Upper). Roentgenogram shows minimal deformity of left hip following coxa plana.

Patient is a young adult, asymptomatic and fully active.

Fic. 9 (Lower). Roentgenogram shows severe residual deformity of right hip in early adult-hood. Patient has limited hip motion, mild limp, and some pain. Increasing difficulty may be

expected as degenerative changes advance.

ARTICLES 989

supply. Gall and Bennett,’4 before Ponseti,

also felt that coxa plana is a “disease not localized to the femoral epiphysis.”

Finally, some broad-minded authors,

notably King” and Sundt, have concluded that coxa plana may well have no single specific cause but may in various instances

result from different abnormalities.

WHAT IS THE FATE OF PATIENTS WITH COXA PLANA?

With the usual resilience of childhood,

most patients, having recovered from the

disease, go happily, busily, and often ath-leticaily through adolescence even though their femoral heads may be deformed and

their hip motion consequently restricted. Prior to their late teens, patients we have

followed have had virtually no symptoms. The evidence that this happy state of affairs does not always continue is only now be-ginning to appear, as long-term studies

become possible. Except from the roentgen-ographic aspect, an accurate assay of end results of coxa plana cannot be made before

the patients have reached maturity.

Ratliff’6 reports on 50 cases followed from

11 to 30 years, carefully evaluated clinically and roentgenographically. Only one-third were normal or nearly so, while about one-fourth were having significant pain and

disability, along with degenerative changes at the hip by roentgenogram. This author cites Branciforti and Montina who studied

12 cases followed an average of 24 years

and concluded that “the fate of these hips is a severe one.”

Goff describes the “end results” in 65 of

his cases followed apparently for 2 to 30

years after bone healing had become

com-plete. Roentgenographically, very few pa-tients had normally spherical femoral heads, while clinically, slightly more than half could be graded excellent or good while the

rest were fair or poor.

In another study, equally difficult to in-terpret because it lacked distinction be-tween short- and long-term follow-up

stud-ies, Mindell and Sherman27 found that most patients had some residual effects from their disease, but were not disabled.

Legg’s report’8 of end results dealt with

40 cases followed for 10 years or more.

While authoritative, it was completely un-detailed. He advised that the majority of

patients will tire easily but none will be incapacitated, and that slightly more than half will have a limp.

In our study the number of patients

followed into the mature years is

inade-quate to be anything more than suggestive (Table VI). A patient “with symptoms” is one who has discomfort other than

occa-sional mild ache. Most of these persons had a perceptible limp and real restriction of motion; all had poorly shaped femoral heads. About one-third of the patients still

under 21 years were symptomatic, while four of the five older patients were having

some difficulty.

Although disagreement on other points is rampant, all students of coxa plana concur that the best end results are found among

those who have tile disease at a very early age-particularly those affected prior to 5

years of age. Our experience is similar. Although many patients, when they reach adulthood, will have good hips, few will

be free of symptoms and some will be crippled. Those who have pain and limp benefit by heat, salicylates, and by limiting their activities. Physical therapy often is a useful adjunct. When these measures prove

inadequate, surgery frequently is advised.

We prefer arthrodesis of the hip for uni-lateral deformity; it provides a sound

pain-TABLE VI

AGE AND LATE SYMPTOMS

Age at Follow-up (yr) Number Number With ‘Symptoms

15 4 1

16 3 1

17 2 0

18 3 1

19 2 2

20 3 1

21 2 2

26 1 1

27 2 1

990 RYDER-COXA PLANA

less weight-bearing limb. Surprisingly little limp results from obliteration of one hip

joint. If both hips are involved an arthro-plasty may be considered.

HOW SHOULD COXA PLANA BE

TREATED?

Here is a thorny medical problem comphi-cated by the social, psychologic and eco-nomic factors common to the treatment of

chronic illness in childhood.

In our review of the course of coxa

plana we have seen that when the afflicted

child comes to us he has a dead femoral head-a situation quite like that faced by the internist whose patient has had a

myo-cardial infarction. How rapidly the head becomes ischemic we do not know, nor do we know what measures might prevent

necrosis could its onset be anticipated.

Our problem thus becomes one of super-vising the patient while nature repairs the

damage. Since we start with an avascular femoral head, we might expedite recovery if we could bring new vessels to the area. This could be done by making holes

through the epiphyseal cartilage so that the rich blood supply of the neck could spread into the head. Howorth, notably, has done this by a “drilling” operation. He reported that the procedure shortened con-valescence when done in 50 cases of coxa

plana. Steele29 enlarged the operation by removing all the necrotic bone from the

head and packing the defect with bone chips. He also felt that this procedure

shortened the disease. Drilling through the neck into the head seemed logical to Jon-s#{228}ter,although he apparently had not done

it. He emphasized that any such procedure must be done early in the disease if it is

to have any value. The actual usefulness of this surgical approach is now unproved.

We also have seen that the only cause of later trouble is the deformity of the femoral head which develops slowly during the

disease. Obviously weight-bearing cannot

but favor this flattening, and in the logical sense at least should be prohibited from the moment the diagnosis is made until the

roentgenograms show good progress into

the repair phase. Indeed the logical end-point of this approach should be to

elimi-nate all pressure between femoral head

and acetabulum including that caused by the muscles about the hip, something which

could be approached by continuous traction on the leg.

The essence of modern treatment thus has come to be non-weight bearing, first

pro-posed by Danforth.’#{176} Statistics are

appear-ing which suggest that it is of benefit even in the face of contrary opinions from such

authorities as Platt, Sundt, and particularly Legg, who wrote, “Relief from weight bear-ing has in no way affected the end result.”

The techniques used to obtain non-weight bearing range in complexity from simple rest in bed, to use of crutches with a sling for the affected leg, to non-weight bearing

braces, to bed rest with traction, to pro-longed retention of the patient in a special abduction-traction frame. All of these are

used in various combinations and sequences. Most of our patients were treated by bed rest for a few months up to 2 years, usually

followed by a period on crutches. A number had had the drilling operation of Howorth followed by bed rest. Some used crutches and sling throughout the disease, but with

a conscientiousness that was often

question-able. In view of tile multiplicity of methods,

the various stages at which treatment began,

and the inherent unpredictability of the disease, we have been quite unable to prove

the superiority of any non-weight bearing

technique over the others. We can report, however, that nine patients who walked

through the disease all had poor hips finally. Essentially this is also the evidence against weight bearing reported by Mindell and Sherman, who found bad results in 10 of 13 untreated cases, and by Ratliff

whose 9 untreated cases in 50 had the worst hips.

Prolonged bed rest with traction has given “vastly improved early end results” in 12 cases as judged by a strict roentgeno-graphic method compared with 12 treated

by crutches, according to Pedersen and McCarroll.” Pike3’ and Goff favor a method

ARTICLES 991

keeping tile patient in a large metal frame.

On the contrary, Mindell and Sherman found no superiority of nonambulatory

treatment over ambulation witilout weight

bearing on tile diseased side. Broder agreed with this view. One easily recognizes the social, psvchologic, and economic implica-tions of these strict techniques, which are

usually impractical except by prolonged institutionalization.

\Ve believe that better understanding of

coxa plana will eventually enable us to pre-vent the disease, just as better understand-ing of coronary arteriosclerosis may enable tis to prevent myocardial infarction. That there will be a “cure” seems doubtful.

At present we subscribe to non-weight hearing, from tile time of diagnosis until

healing is well advanced, as the cardinal principle of treatment. It is logical and ap-parelltly beneficial. At the New York

Ortho-paedic Hospital our current practice is simple: bed rest until painless hip motion is

achieved, followed by use of crutches and sling. Children with bilateral disease are merely kept in bed. Perhaps this approach often implies an unwarranted faith in the

reliability of small boys and girls.

We believe that there are still grounds for

controversy between the school which favors the more complex traction and brace techniques, and the advocates, including

ourselves, of the simpler methods. If we are proved wrong, we shall hasten to capitu-late.

REFERENCES

1. Legg, A. T.: An obscure affection of the hip-joint. Boston M. & S.

J.,

162:202, 1910.

2. Calve, j.: Stir tine forme particuhi#{232}re de pseudo-coxalgie greff#{233}e stir des d#{233}forma-tions caract#{233}ristiques de l’extr#{233}mit#{233}

su-p#{233}rieuredu femur. Rev. chir., Paris, 42: 54, 1910.

3. Perthes, C.: Uber Arthritis deformans

juvenilis. Deutsche Ztschr. Chir., 107: 111, 1910.

4. Coff, C. W.: Legg-Calv#{233}-Perthes

Svn-drome and Related Osteochondroses of

Youth. Springfield, Thomas, 1954. 5. Broder, H.: The late results in

Legg-Perthes’ disease and factors influencing them: a study of one hundred and two

cases. Bull. Hosp. Joint Dis., 14:194,

1953.

6. Sundt, H. : The aetiology of

pseudo-coxaigia. Lancet, 1:1153, 1921.

7. Haythorn, S. R. : Pathological changes

found in material removed at operation in Legg-Calv#{233}-Perthes disease.

J.

Bone

& Joint Surg., 31-A:599, 1949.

8 Lippmann, R. K. : The pathogenesis of

Legg-Calv#{233}-Perthes’ disease based upon the pathologic findings in a case. Am.

J.

Surg., 6:785, 1929.

9. Jonsater, S.: Coxa plana: A histo-pathologic

and arthrografic study. Acta orthop. scandinav., Suppl. 12, 1953.

10. Waldenstr#{246}m, H. : The definite form of

coxa plana. Acta radiol., 1 :384, 1922. 11. Howorth, M. B.: Coxa plana.

J.

Bone &

Joint Surg., 30-A:601, 1948.

12. Kidner, F. C. : Causes and treatment of

Perthes’ disease. Am.

J.

Orth. Surg., 14: 339, 1916

13. Phemister, D. B., Brunschwig, A., and Day, L.: Streptococcal infections of the epiphyses and short bones. Their rela-tion to Kohler’s disease of the tarsal navicular, Legg-Perthes’ disease, and Kienboch’s disease of the os lunatum. J.A.M.A., 95:995, 1930.

14. Durham, H. A., and Outland, T. A.: Blood calcium and phosphorus in Perthes’ dis-ease; a new conception of the etiology;

preliminary report.

J.

Bone & Joint

Surg., 10:301, 1928.

15. Buchman,

J.:

A r#{233}sum#{233}of the osteo-chondritides. Surg., Gvnec. & Obst., 49:

447, 1929.

16. Cavanaugh, L. A., Shelton, E. K., and Sutherland, R.: Metabolic studies in osteochondritis of the capital femoral epiphvsis.

J.

Bone & Joint Surg., 18: 957, 1936.

17. Schaefer, R. L., and Purcell, F. H.: Juve-nile osteochondreal (chondroepiphvsitis)

hypothyroidism. Am.

J.

Surg., 54:589,

1941.

18. Ciii, A. B.: Relationship of Legg-Perthes’ disease to the function of the thyroid

gland.

J.

Bone & Joint Surg., 25:892,

1943.

19. Katz,

J.

F.: Protein-bound iodine in Legg-Calv#{233}-Perthes disease.

J.

Bone & Joint Surg., 37-A:842, 1955.

20. Kolodnv, A.: The architecture and the blood supply of the head and neck of the femur and their importance in the pathology of fractures of the neck.

J.

Bone & Joint Surg., 7:575, 1925. 21. Zemansky, A. P., Jr., and Lippmann,

R. K.: The importance of the vessels in

992 RYDER-COXA PLANA

femur during the period of growth and their possible relationship to Perthes’ disease. Surg., Gynec. & Obst., 48:461, 1929.

22. Platt, H. : Pseudo-coxalgia: A clinical and

radiographic study. Brit.

J.

Surg., 9: 366, 1922.

23. Ponseti, I. V.: Legg-Perthes disease. Ob-servations on pathological changes in two cases.

J.

Bone & Joint Surg., 38-A: 739, 1956.

24. Gall, E. A., and Bennett, C. A.: Osteo-chondritis deformans of hip (Legg-Perthes disease) and renal osteitis fibrosa

cystica; report of a case with anatomic studies. Arch. Path., 33:866, 1942.

25.

King, E. S.

J.:

Localized Rarefying Con-ditions of Bone as Exemplified by Legg-Perthes’ Disease, Osgood-Schlatter’s Dis-ease, K#{252}mmell’s Disease and Related Conditions. London, Arnold, 1935. 26. Ratliff, A. H. C.: Pseudocoxalgia. A study

of late results in the adult.

J.

Bone & Joint Surg., 38-B:498, 1956.

27. Mindell, E. R., and Sherman, M. S.: Late results in Legg-Perthes disease.

J.

Bone

& Joint Surg., 33-A: 1, 1951.

28. Legg, A. T.: The end results of coxa plana.

J.

Bone & Joint Surg., 9:26, 1927. 29. Steele, P. B.: Further report on the

opera-tive treatment of Perthes’ disease, in Lectures on Peace and War Orthopedic Surgery, The American Academy of Orthopaedic Surgeons. Ann Arbor, Ed-wards Brothers, 1943.

30. Danforth, M. S.: The treatment of Legg-CalvC-Perthes disease without weight-bearing.

J.

Bone & Joint Surg., 16:516,

1934.

31. Pedersen, H. E., and McCarroll, H. R.: Treatment in Legg-Perthes disease.

J.

Bone & Joint Surg., 33-A:591, 1951.

32. Pike, M. M.: Legg-Perthes disease; a method of conservative treatment.

J.

Bone & Joint Surg., 32-A:663, 1950.

SUMMARIO IN INTERLINGUA

Coxa Plan

Le studio de 104 casos de coxa plan revelava le declaration del morbo occurrente a etates de inter 23 e 133 annos. Un medietate del pa-tientes habeva etates de inter 4 e 6 annos. Omne le patientes, con un sol exception, es-seva blancos. Le exception esseva un negro. Le

proportion de masculos a femininas esseva cinque a un. Le serie includeva 16 casos bila-teral, omnes in pueros. Le coxa sinistre e le coxa

dextere esseva efficite con equal frequentia.

Claudication e dolor, communmente

pre-sente durante 3 a 6 menses, esseva le

sympto-mas inducente le presentation al consulta medi-cal. Dolor in motion coxal, spasmo, e restringi-mento de abduction e rotation esseva le

cha-racteristic constatationes physic. Le examine roentgenographic establiva le diagnose in

prac-ticamente omne le patientes del serie. In casos de affection bilateral, symptomas e constata-tiones unilateral esseva he regula. Le diagnose bilateral resultava del examine roentgeno-graphic.

Le studios bioptic e arthrographic de Jonsater

ha monstrate que in le stadio initial le

roent-genogramma revela necrosis del osso in le epi-physe del capite femoral, ben que he

conforma-tion del capite total es spheric. In he stadio de Iragmentation le reparo del osso ha comenciate, e le conformation del capite non es marcate-mente alternate. In le stadio de reparo osso nor-mal retorna al capite femoral, e planification del superficie articular deveni conspicue. Final-mente he stadio definite superveni, con matur structura ossee e permanentia de conformation del capite. Le integre processo es variabile in su severitate.

Le majoritate del autores es de accordo que

le causa immediate de coxa plan es dysfunction del provision de sanguine at capite femoral. Sub le mehior conditiones iste provision es precari.

Q

ual factores specific interrumpe le circulation non es cognoscite. Secundo le hypothese de Ponseti, que es basate super datos histopa-thologic, he lesion primari in coxa plan es in.fir-mation e disruption del platta capital del

femore, con affection secundari del vasos epi-physal in br passage a transverso ille structura. Le nunc disponibile studios del resultatos

final indica que he sol residuo de coxa plan in adultos es un deformitate del articulation coxal con consequente alterationes degenerative. Isto es responsabile pro le facto que inter un medie-tate e duo tertios del patientes retine anormal

articulationes que produce symptomas e inva-hiditates de grado leve o sever.

Durante le phase active del morbo, be

1957;19;979

Pediatrics

Charles T. Ryder, John D. LeBouvier and Rosamond Kane

COXA PLANA

Services

Updated Information &

http://pediatrics.aappublications.org/content/19/6/979

including high resolution figures, can be found at:

Permissions & Licensing

http://www.aappublications.org/site/misc/Permissions.xhtml

entirety can be found online at:

Information about reproducing this article in parts (figures, tables) or in its

Reprints

http://www.aappublications.org/site/misc/reprints.xhtml

1957;19;979

Pediatrics

Charles T. Ryder, John D. LeBouvier and Rosamond Kane

COXA PLANA

http://pediatrics.aappublications.org/content/19/6/979

the World Wide Web at:

The online version of this article, along with updated information and services, is located on

American Academy of Pediatrics. All rights reserved. Print ISSN: 1073-0397.